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martes, 15 de marzo de 2016

Phenylephrine (pure alpha-1 agonist)

This is the first of a series of four posts about vasopressors and hemodynamics. The first step is to explore the physiology of a pure alpha-1 agonist (phenylephrine).

Make no mistake, I’m not very fond of phenylephrine. I rarely use it (mostly for hypotensive atrial fibrillation). However, understanding phenylephrine is a prerequisite to understanding related vasopressors, particularly midodrine and norepinephrine.

Evidence regarding phenylephrine consists of a patchwork of often contradictory human and animal studies, based mostly on surrogate endpoints. Thus, this post is framed as an alternative viewpoint: a perspective which remains debatable.

Norepinephrine is similar to phenylephrine (norepinephrine is equivalent to phenylephrine plus some beta-1 stimulation). In some situations the two drugs may function in an identical fashion.

Like norephrine, phenylephrine can cause venoconstriction, thereby increasing venous return to the heart.

Phenylephrine can affect cardiac output in a variety of ways:

Increased preload may increase cardiac output

Increased afterload and reflex bradycardia may reduce cardiac output.

The effect of phenylephrine on cardiac output varies depending on the clinical context.

The most common mechanism whereby phenylephrine reduces cardiac output may be reflex bradycardia. Thus, an inappropriately low heart rate in a shocked patient on phenylephrine suggests that cardiac output is being suppressed.